Previous work from this laboratory has documented deficiencies of the cell mediated immune response in human an experimental murine leprosy. In work submitted for publication, we have demonstrated a perturbation of lymphocyte recirculation in M. lepraemurium infected rats after intravenous infusion of syngeneic, radioactively labelled thoracic duct cells from normal animals. In addition, we have quantitated the theta-alloantigen bearing lymphocyte population in spleen, lymph node and peripheral blood of leprous rodents as compared with normal controls. Work at present is centered in two areas. In the first project we are studying the kinetics of lymphocyte mobilization by the synthetic polyanion, polymethacrylic acid (PMAA), in both normal and leprous rodents. Since lymphocyte circulation is seriously disturbed in the latter, it might be expected that mobilization kinetics following injection of PMAA would also be disturbed. As a second project, in collaboration with Dr. Peter Ward, we are examining the evidence for defective leukotaxis in patients with lepromatous leprosy. Sera from some patients with this disease contain a chemotactic inhibitor that irreversibly inhibits a variety of chemotactic factors. The nature of this inhibitor factor appears to be similar to a serum factor recently termed chemotactic factor inactivator. The presence of this factor in leprosy sera may be responsible for some of the defects of cellular inflammatory responses found in patients with lepromatous leprosy. Bibliographic references: Bullock, W.E.: Anergy and Infection. Advances in internal Medicine, Volume 21, Little, Brown and Company, Boston, 1975. Bullock, W.E.: Specificity of immunodeficiency in leprosy and other infections. In Progress in Immunology II, Volume 5 Clinical Aspects II, page 193, Eds. L. Brent and J. Holborow, North Holland, Amsterdam, 1974.